Several platinum coordination complexes such as cis-diamminedichloroplatinum (II) (cisplatin) and diamine[1,1-cyclobutanedicarboxylato]-O,O′-platinum (II) (carboplatin) are currently used in chemotherapy of neoplastic diseases. These complexes of a non-essential heavy metal, exhibit a remarkable antitumor effectiveness and a broad spectrum of activity. It is widely believed that the antitumor activity of platinum drugs is a consequence of their interaction with DNA. Cisplatin binds readily to guanine residues of DNA molecules. Cisplatin has proved very successful in the treatment of a variety of human solid tumors such as genitourinary and gynecologic tumors as well as head, neck and lung tumors. Unfortunately, the development of cellular resistance to cisplatin in mammalian cells is common and is believed to occurs via, four main mechanisms: (a) increased efficiency of repair of platinum-DNA lesions, (b) increased inactivation of drug by elevated levels of cellular low-molecular weight thiols, particularly glutathione, (c) metallothionein, and (d) decreased cellular uptake of drug. Its toxic effects, particularly kidney toxicity and neurotoxicity, also limit the clinical utility of the drug. It is noteworthy that carboplatin is less toxic than cisplatin and can be given at a much higher dose (up to 2000 mg/dose for carboplatin as compare to a typical dose of 100 mg/day for cisplatin).
More recently, two other platinum (II) derivatives were approved for use in some countries. (trans-L-diaminocyclohexane)oxalatoplatinum(II) (oxaliplatin (4)) has been approved for the secondary treatment of metastatic colorectal cancer in France and other European countries. cis-diammine-glycoloato-O,O′-platinum (II) (nedaplatin (5)) has received approval for use in Japan. Unfortunately, oxaplatin and nedaplatin have not shown any distinct advantages over cisplatin and carboplatin. The search for platinum complexes with a broader spectrum of activity, less toxicity, improved clinical effectiveness against tumors characterized by intrinsic or acquired resistance to cisplatin is ongoing.
Scheme 1: Structure of the known platinum (II) complexes.

The following literature reviews present a broad overview of the actual knowledge of platinum-based antitumor agents as well as of their mechanism of action:
E, Wong and C. M. Giandomenico, << Current Status of Platinum-Based Antitumor Drugs >>, Chemical Review, 99, 2451–2466 (1999)
E. R. Jamieson and S. J. Lippard, << Structure, Recognition, and Processing of Cisplatin-DNA Adducts >>. Chemical Review, 99, 2467–2498 (1999)
J. Reedijk, << Why Does Cisplatin Reach Guanine-N7 with Competing S-Donor Ligands Available in the Cell?>>, Chemical Review, 99, 2499–2510 (1999)